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Biomedical subjects

Akitaka Tsujikawa

Publications and source records attributed to Akitaka Tsujikawa.

18 recordsLinked to original sources
PubMed2006

Pigment epithelial detachment in polypoidal choroidal vasculopathy.

PURPOSE: To study the morphological features of serosanguineous pigment epithelial detachments (PEDs) with accompanying polypoidal lesions in eyes with polypoidal choroidal vasculopathy (PCV). DESIGN: Retrospective observational case series. METHODS: For this observational case study, we retrospectively reviewed 93 consecutive eyes of 85 patients with PCV. The lesions in eyes with PCV were examined with indocyanine green angiography (IA) and optical coherence tomography (OCT). RESULTS: Of 93 eyes with PCV, 51 eyes (55%) had serous or hemorrhagic PEDs. Of these 51 eyes, a notch in the PED was found in 27 eyes (53%) by angiography, most of which showed polypoidal lesions by IA that corresponded in location to the notch observed by angiography. Polypoidal lesions were detected outside the PED in one eye (2%), at the margin of the PED in 33 eyes (65%), and inside the PED in 12 eyes (24%). OCT revealed that PED had a notch observed tomographically in 29 eyes (57%), most of which corresponded in location to polypoidal lesions seen by IA. In eight eyes, polypoidal lesions, which were adherent to the inner surface of the serous PED, appeared to be detached from the Bruch membrane and the choroid. CONCLUSIONS: Polypoidal lesions are located at the margin of PED and make a notch in the accompanying PED that is visible by angiography and tomographically. When the polypoidal lesions have increased exudate, the fluid from the lesions infiltrates under the polypoidal lesions themselves, which results in the lesions detaching from the Bruch membrane and appearing to be located inside the PED.

Aged↗
PubMed2006

Photoreceptor status after resolved macular edema in branch retinal vein occlusion treated with tissue plasminogen activator.

PURPOSE: To evaluate the integrity of photoreceptors in macular edema (ME) associated with branch retinal vein occlusion after intravitreal tissue plasminogen activator. DESIGN: Retrospective, interventional case series. METHODS: Nineteen eyes with ME by branch retinal vein occlusion were treated with intravitreal tissue plasminogen activator injection. We assessed visual acuity (VA) and the presence or absence in the fovea of a third high reflectance band (HRB) by optical coherence tomography at the final visit. RESULTS: No differences were found in age, preoperative VA, and foveal thickness between the groups with or without the third HRB. After treatment, the mean VA improved significantly (P < .05) in both groups. At the final visit, the mean VA in the group without HRB was significantly poorer than the group with HRB (P = .0042); foveal thickness did not differ between the groups. CONCLUSIONS: The integrity of the third HRB in the fovea is associated with VA after the resolution of ME.

Female↗
PubMed2006

Recurrent bleeding after photodynamic therapy in polypoidal choroidal vasculopathy.

PURPOSE: To report a case of recurrent bleeding after photodynamic therapy (PDT) in an eye with polypoidal choroidal vasculopathy (PCV). DESIGN: Interventional case report. METHODS: A 73-year-old man was treated in the left eye for PCV with PDT. RESULTS: Two weeks after PDT, his left eye showed extensive subretinal hemorrhage, with a slight vision loss. Three months after PDT, subretinal hemorrhage was almost absorbed. He received a second session of PDT to the remaining choroidal neovascularization. Two weeks thereafter, his left eye showed massive suprachoroidal hemorrhage with further vision loss. One month after the second PDT, visual acuity was decreased to no light perception as a result of massive vitreous hemorrhage. Although the patient underwent pars plana vitrectomy, visual acuity in the left eye remained hand motion as a result of massive suprachoroidal hemorrhage. CONCLUSIONS: Ophthalmologists and patients should be aware of the risk of massive bleeding after PDT in eyes with PCV.

Aged↗
PubMed2006

Polypoidal choroidal vasculopathy with choroidal vascular hyperpermeability.

PURPOSE: To describe the incidence and clinical characteristics of polypoidal choroidal vasculopathy (PCV) associated with choroidal vascular hyperpermeability. DESIGN: Retrospective observational case series. METHODS: We reviewed the medical records of 122 consecutive eyes with PCV and 106 consecutive eyes with exudative age-related macular degeneration (AMD). Fluorescein angiography and indocyanine green (ICG) angiography were performed using a confocal scanning laser system. In the midphase of ICG angiography, we evaluated choroidal vascular hyperpermeability, which is recognized as one of the characteristic findings in central serous chorioretinopathy (CSC). Choroidal vascular hyperpermeability appeared as multifocal patchy areas of hyperfluorescence with blurred margins within the choroid that increased in intensity with time after injection of the dye. RESULTS: Of 122 eyes with PCV, 12 (9.8%) eyes of 10 patients exhibited multifocal choroidal hyperfluorescence in the midphase of ICG angiography, whereas two (1.9%) of 106 eyes with exudative AMD showed a similar appearance (P = .013). Of the 12 eyes in 10 patients with PCV that demonstrated multifocal choroidal hyperfluorescence, we also noted that the early phase of ICG angiography showed choroidal filling delay in seven eyes (58%) and venous dilation in 12 eyes (100%). Four of these 12 eyes (33%) had a medical history of CSC, and nine (90%) of the 10 patients revealed multifocal choroidal hyperfluorescence bilaterally. CONCLUSIONS: Multifocal choroidal hyperfluorescence seen by ICG angiography occurs more frequently in eyes with PCV than in those with AMD. Choroidal vascular hyperpermeability, reportedly a characteristic finding in CSC, might be one of the risk factors of PCV.

Aged↗
PubMed2006

Fellow eye of patients with retinal detachment associated with macular hole and bilateral high myopia.

PURPOSE: To estimate the risk of retinal detachment in the fellow eye of patients with bilateral high myopia who had retinal detachment associated with macular hole (MH-RD) in one eye. METHODS: The present study examined retrospectively 56 patients with bilateral high myopia who had MH-RD. To determine the incidence of involvement of the fellow eye, patients who completed a follow up of 12 months or longer were eligible for the current study. RESULTS: Of 56 patients with MH-RD due to high myopia, 54 had unilateral detachment at presentation and two had bilateral detachment. Of the 54 highly myopic fellow eyes without retinal detachment at presentation, 37 eyes underwent 12 or more months of documented follow up. Mean follow up after initial surgery to the primary eye was 6.5 +/- 4.9 years. During follow up, a macular hole without retinal detachment was noted in one (2.7%) of these 37 eyes. Three other eyes (8.1%) had MH-RD at 1, 2 and 7 years, respectively, after the initial surgery to the primary eye. At the final visit, 12 eyes (32%) had visual acuity of > or =6/9, whereas 12 eyes (32%) had visual acuity of < or =6/60. CONCLUSIONS: When patients with bilateral high myopia have MH-RD in one eye, they would be expected to be at increased risk of retinal detachment in the fellow eye.

Aged↗
PubMed2005

Retinal cystoid spaces in acute Vogt-Koyanagi-Harada syndrome.

PURPOSE: Exudative retinal detachment in acute Vogt-Koyanagi-Harada syndrome often is associated with subfoveal yellowish round structures. This report describes the incidence and clinical characteristics of these structures. DESIGN: Interventional case series. METHODS: We reviewed the fundus photographs and medical records of 35 eyes of 19 Japanese patients with bilateral diffuse choroiditis at the onset of acute Vogt-Koyanagi-Harada syndrome. RESULTS: All eyes showed subretinal fluid in the posterior pole. In addition, yellowish round structures were seen in 15 eyes (43%). Most of the yellowish structures were subfoveal in location and ranged in size from less than 1 disk diameter to 3 disk diameters. In 6 eyes with these structures, optical coherence tomography showed liquid accumulation in the retina or thin walls, which seemed to separate the cystoid spaces from the subretinal fluid. Late-phase fluorescein angiography showed pooling of dye within these structures as well as within the subretinal fluid. Immediately after corticosteroid administration was initiated, these structures began to be less obvious, and they disappeared completely within several days; there was a concomitant reduction in the subretinal fluid. At the initial visit, visual acuity in eyes with these yellowish structures was slightly less than that in eyes without them, but no differences in visual acuity were found during the period of follow-up. CONCLUSION: Subfoveal yellowish round structures may be a common feature in acute Vogt-Koyanagi-Harada syndrome. However, they appear to have only a minor (if any) effect on visual prognosis.

Acute Disease↗
PubMed2004

Simvastatin inhibits leukocyte accumulation and vascular permeability in the retinas of rats with streptozotocin-induced diabetes.

Leukocytes play important roles in the pathogenesis of diabetic retinopathy. Recently, 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors have been reported to exert various effects in addition to their lipid-lowering ability. We investigated the effects of simvastatin, a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor, on leukocyte-induced diabetic changes in retinas. Diabetes was induced in Long-Evans rats with streptozotocin, and simvastatin administration was begun immediately after the induction of diabetes. Two weeks of treatment with simvastatin suppressed significantly the number of leukocytes adhering to retinal vessel endothelium and the number of leukocytes accumulated in the retinal tissue by 72.9% and 41.0%, respectively (P < 0.01). The expression of intercellular adhesion molecule-1 (ICAM-1) and the CD18 (the common beta-chain of ICAM-1 ligands) were both suppressed with simvastatin. The amount of vascular endothelial growth factor in the retina was attenuated in the simvastatin-treated group. To evaluate the effects of simvastatin on leukocyte-induced endothelial cell damage, vascular permeability in the retina was measured with fluorescein-labeled dextran. Treatment with simvastatin markedly reduced retinal permeability (P = 0.014). This suggests that simvastatin attenuates leukocyte-endothelial cell interactions and subsequent blood-retinal barrier breakdown via suppression of vascular endothelial growth factor-induced ICAM-1 expression in the diabetic retina. Simvastatin may thus be useful in the prevention of diabetic retinopathy.

Animals↗
PubMed2004

Pars plana vitrectomy for vitreous opacity associated with ocular sarcoidosis resistant to medical treatment.

OBJECTIVE: To examine the results of pars plana vitrectomy for nonclearing vitreous opacities associated with ocular sarcoidosis that is resistant to corticosteroid treatment. METHODS: Eight consecutive patients (11 eyes) with vitreous opacities and uveitis associated with sarcoidosis were studied. All patients were resistant to or intolerant of corticosteroid therapy. All eyes underwent pars plana vitrectomy, followed by evaluation of visual acuity and recording of the grade of inflammation and complications. RESULTS: Seven eyes had gained two or more lines of Snellen visual acuity six months postoperatively; visual acuity remained unchanged in the other four eyes. Vitreous inflammation was reduced in all cases. Severe postoperative inflammation did not recur in any eyes. Five eyes developed visually significant cataracts and underwent cataract extraction and intraocular lens insertion within 8-30 months. Based on slit-lamp biomicroscopy and fluorescein angiography, preoperative cystoid macular edema in five eyes resolved or improved within six months after vitrectomy. Postoperative complications included elevated intraocular pressure in three eyes, cataract formation in six eyes, epiretinal membrane formation in one eye, and choroidal neovascularization in one eye. None of the patients developed cystoid macular edema postoperatively. Only three patients received systemic corticosteroids after surgery. At the final visit, only one patient required systemic corticosteroid therapy. CONCLUSIONS: Pars plana vitrectomy appears to have beneficial effects on restoring vision, stabilizing vitreous inflammation, and reducing systemic corticosteroid requirements in eyes with thick vitreous opacities associated with sarcoidosis that is resistant to medical treatment.

Adult↗
PubMed2004

Platelets adhering to the vascular wall mediate postischemic leukocyte-endothelial cell interactions in retinal microcirculation.

PURPOSE: Recent evidence suggests that platelets play a major role in ischemia-reperfusion injury, not only through thrombus formation but also through participation in inflammatory reactions with leukocytes. This study was designed to investigate the contribution of platelets in leukocyte recruitment to inflamed regions in vivo. METHODS: Thrombocytopenia was produced in male Long-Evans rats by intravenous injection of anti-platelet serum at 4 hours before ischemia-reperfusion. Leukocyte behavior in retinal microcirculation was evaluated with acridine orange digital fluorography. Expression of P-selectin in the postischemia retina was investigated by reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry. After 14 days of reperfusion, ischemia-induced retinal damage was evaluated histologically. RESULTS: Leukocyte rolling along major retinal veins of thrombocytopenic rats was dramatically suppressed, and subsequent leukocyte accumulation in the postischemia retina was also significantly reduced (72.3%; P < 0.001) at 24 hours after reperfusion. Although RT-PCR revealed no significant reduction of P-selectin mRNA in platelet-depleted rat retina after transient ischemia, immunohistologic examination showed suppression of P-selectin expression on the vascular wall. Another immunologic examination using anti-platelet antibody detected adherent platelets, which can also express P-selectin on their surfaces, on postischemic vascular endothelium in vehicle-treated retina. Moreover, blockage of platelet glycoprotein IIb/IIIa resulted in substantial inhibition of leukocyte rolling. In addition, histologic examination showed the participation of platelets in retinal ischemia-reperfusion injury. CONCLUSIONS: This study demonstrated that the expression of P-selectin on platelets may contribute to the recruitment of leukocytes to tissues after ischemia.

Acridine Orange↗
PubMed2003

Argatroban attenuates leukocyte- and platelet-endothelial cell interactions after transient retinal ischemia.

BACKGROUND AND PURPOSE: Argatroban, a direct thrombin inhibitor, has been shown to reduce neural injury after transient cerebral ischemia. It has also been reported that this neuroprotective effect results from an anticoagulant function. This study was designed to evaluate quantitatively the inhibitory effects of argatroban on leukocyte- and platelet-endothelial cell interactions after transient retinal ischemia. METHODS: Retinal ischemia was induced for 60 minutes in male Long-Evans rats by temporary ligation of the optic sheath (n=342). Argatroban was administered just after induction of ischemia. Leukocyte and platelet behavior in the retinal microcirculation was then evaluated in vivo with scanning laser ophthalmoscopy. The expression of P-selectin and intracellular adhesion molecule-1 (ICAM-1) was evaluated by reverse transcription-polymerase chain reaction. After 10 days of reperfusion, ischemia-induced retinal damage was evaluated histologically. RESULTS: Treatment with argatroban suppressed leukocyte-endothelial cell interactions; the maximum numbers of rolling and accumulated leukocytes were reduced by 90.1% (P<0.05) and 58.7% (P<0.05), respectively, at 12 hours after reperfusion. Treatment with argatroban also suppressed platelet-endothelial cell interactions; the maximum numbers of rolling and adhering platelets were reduced by 91.8% (P<0.01) and 78.9% (P<0.01), respectively, at 12 hours after reperfusion. The expression of P-selectin and ICAM-1 mRNA was suppressed significantly in the argatroban-treated retinas (P<0.01). Histologic examination demonstrated the protective effect of argatroban on ischemia-induced retinal damage (P<0.01). CONCLUSIONS: Argatroban treatment suppressed leukocyte- and platelet-endothelial cell interactions after transient retinal ischemia. This inhibitory effect on postischemic blood cell-endothelial cell interactions might partially contribute to its neuroprotective effects.

Animals↗
PubMed2003

Platelets accumulate in the diabetic retinal vasculature following endothelial death and suppress blood-retinal barrier breakdown.

Platelet microthrombi are present in the diabetic retinal vasculature of humans and rodents; however, the mechanisms and consequences of their presence have not been defined. The current study demonstrates that platelet containing microthrombi accumulate in the retinal vasculature of the rat within 2 weeks of experimental diabetes, a timepoint at which leukocyte-mediated endothelial cell injury and death are known to occur. Platelet accumulation increased with the duration of diabetes, and crossover experiments revealed that maximal platelet accumulation required both diabetic platelets and a diabetic endothelium. Platelet accumulation also coincided with the expression of Fas and FasL in the diabetic retina. When endothelial cell apoptosis was inhibited with an anti-FasL neutralizing antibody, platelet accumulation was effectively suppressed. When platelets were depleted from the systemic circulation with an anti-platelet antibody, blood-retinal barrier breakdown worsened in the diabetic animals. These findings suggest that platelet accumulation in the diabetic retinal vasculature is secondary to endothelial cell death and serves, in part, to suppress blood-retinal barrier breakdown.

Animals↗
PubMed2003

Inhibitory effects of antithrombin III on interactions between blood cells and endothelial cells during retinal ischemia-reperfusion injury.

PURPOSE: Infiltrating leukocytes have long been widely thought to be key mediators of ischemia-reperfusion injury. Recently, however, evidence suggests that platelets accumulating in postischemic tissues also contribute to ischemia-reperfusion injury because of their inflammatory properties and promotion of formation of thrombi. This study was designed to evaluate quantitatively the inhibitory effects of antithrombin (AT)-III on the interactions between blood cells and retinal endothelial cells in vivo after transient retinal ischemia. METHODS: Transient retinal ischemia was induced for 60 minutes in male Long-Evans rats by ligation of the optic nerve. AT III (250 U/kg) was administered intravenously just after induction of ischemia. Leukocyte and platelet behavior in the retina was evaluated in vivo with a scanning laser ophthalmoscope. Expression of P-selectin and intracellular adhesion molecule (ICAM)-1 in the postischemic retina was investigated by reverse transcription-polymerase chain reaction and immunohistochemistry. After 14 days of reperfusion, ischemia-induced retinal damage was evaluated histologically. RESULTS: Administration of AT III significantly inhibited leukocyte rolling along the major retinal veins and subsequent accumulation of leukocytes in the postischemic retina. Furthermore, the maximum number of rolling and adherent platelets was reduced by 76% (P < 0.01) and 48% (P < 0.01), respectively, at 12 hours after reperfusion. Immunohistochemical studies also revealed the suppressive effect of AT III on expression of P-selectin and ICAM-1. Finally, histologic examination demonstrated the protective effects of AT III against retinal damage after transient retinal ischemia. CONCLUSIONS: This study demonstrates the inhibitory effects of AT III on leukocyte and platelet recruitment to the postischemic retina, which may account for the neuroprotective properties of this alpha-2 globulin against retinal ischemia-reperfusion injury.

Acridine Orange↗
PubMed2002

Suppression of diabetic retinopathy with angiopoietin-1.

Diabetic retinopathy remains a leading cause of irreversible blindness. A critical early pathology in the disease is the adhesion of leukocytes to the retinal vasculature, a process that occurs, in part, via intercellular adhesion molecule-1. Once leukocyte adhesion occurs, endothelial cell injury ensues, as does blood-retinal barrier breakdown. Here we show that angiopoietin-1 can prevent and reverse these diabetic retinal vascular changes in both new and established diabetes. Angiopoietin-1, when given intravitreally to newly diabetic rats, normalized retinal vascular endothelial growth factor (VEGF) and intercellular adhesion molecule-1 mRNA and protein levels, leading to reductions in leukocyte adhesion, endothelial cell injury, and blood-retinal barrier breakdown. When an adenovirus coding for angiopoietin-1 was given systemically to mice with established diabetes, it similarly inhibited leukocyte adhesion and endothelial cell injury and blood-retinal barrier breakdown. These changes coincided with reductions in retinal eNOS, nitric oxide, Akt (protein kinase B), and MAP kinase activity, known mediators of VEGF bioactivity and leukocyte adhesion. When endogenous VEGF bioactivity was inhibited with a soluble Flt-1/Fc chimera, retinal Akt kinase activity was significantly reduced in vivo. Taken together, these data document new vascular and anti-inflammatory bioactivities for angiopoietin-1 and identify it as the first naturally occurring protein that directly protects the retinal vasculature in diabetes.

Angiopoietin-1↗
PubMed2002

Inflammatory response after scatter laser photocoagulation in nonphotocoagulated retina.

PURPOSE: Macular edema is one of the most serious adverse effects after retinal scatter laser photocoagulation. It has been suggested that the changes in the distribution of retinal blood flow or the inflammatory reaction after photocoagulation may be involved in the pathogenesis of macular edema, but little information is available about its exact mechanism. This study was designed to evaluate quantitatively leukocyte-endothelial cell interactions and vascular permeability in the nonphotocoagulated portions of the retina after partial scatter laser photocoagulation. METHODS: Argon laser photocoagulation was performed in one half of the retina in male pigmented rats (n = 90). In the other half of the retina, leukocyte dynamics after photocoagulation were evaluated in vivo with acridine orange digital fluorography. Retinal vessel permeability was quantified by using Evans blue dye. RESULTS: Scatter laser photocoagulation caused significant inflammatory leukocyte-endothelial interactions not only in the photocoagulated but also in the untreated half of the retina. In the nonphotocoagulated half of the retina, the number of leukocytes rolling along the major retinal veins increased after photocoagulation and peaked at 12 hours (14.3 +/- 4.5 cells/min per vessel). Leukocyte accumulation in the untreated half of the retina increased after photocoagulation, with a peak of 47.5 +/- 13.0 cells/mm(2) 24 hours after photocoagulation. Retinal vascular permeability in the untreated half of the retina gradually increased after photocoagulation. CONCLUSIONS: Scatter laser photocoagulation increased leukocyte rolling and subsequent accumulation in both the photocoagulated and the untreated portions of the retina. The accumulated leukocytes may be involved in the augmented vascular permeability in the untreated retina, resulting in retinal edema after photocoagulation.

Acridine Orange↗
PubMedDate not supplied

Neovascular glaucoma after branch retinal artery occlusion.

BACKGROUND: Neovascular glaucoma (NVG) occurring after branch retinal artery occlusion (BRAO) might not be as rare as previously thought. We report a case of unilateral NVG after BRAO. CASE: A 72-year-old man with chronic heart failure suffered from BRAO in the left eye. Funduscopic examination showed retinal edema and many cotton wool spots in the superotemporal retina. OBSERVATIONS: Five weeks later, he had increased blurring of vision due to a second BRAO in the inferotemporal retina of the left eye. Three days later, he felt pain and had severe visual loss in the left eye. In the presence of angle neovascularization, intraocular pressure (IOP) in the left eye rose to 35 mmHg. Immediate focal photocoagulation to the affected retina diminished the neovascularization and lowered the IOP. CONCLUSION: It is possible for NVG to occur as a complication of BRAO.

Aged↗
PubMedDate not supplied

Visual field defect after radial optic neurotomy for central retinal vein occlusion.

PURPOSE: To evaluate visual field defects after radial optic neurotomy (RON) in eyes with central retinal vein occlusion (CRVO). METHODS: Eight patients (eight eyes) underwent RON for macular edema associated with CRVO. Goldmann perimetry was performed on each patient both before and after surgery. RESULTS: Postoperative Goldmann perimetry showed a temporally located wedge-shaped visual field defect consistent with neural damage secondary to RON in seven eyes (88%). After surgery, the visual field decreased from preoperative values by 7% at 3 months (P = 0.30) and by 21% at 12 months (P = 0.0023). Although three patients (38%) were aware of the postoperative visual field defect, only one patient (13%) considered this defect to be a visual disability. CONCLUSIONS: After RON, most patients showed a postoperative defect in the temporal visual field consistent with the incision to the optic disk. However, this visual field defect appears to be well tolerated by most patients.

Adult↗
PubMedDate not supplied

Triamcinolone acetonide with vitrectomy for treatment of macular edema associated with branch retinal vein occlusion.

PURPOSE: To review the efficacy of a combination of triamcinolone acetonide (TA) injection and pars plana vitrectomy (PPV) for the treatment of macular edema associated with branch retinal vein occlusion (BRVO). METHODS: Seventeen eyes with macular edema associated with BRVO underwent PPV with an intraoperative injection of TA (10 mg) into the vitreous cavity. Residual or recurrent macular edema was treated with postoperative sub-Tenon capsule injections of TA (20 mg). RESULTS: With PPV and an intraoperative injection of TA, 82% of eyes showed rapid reduction of macular edema; foveal thickness decreased from 507 +/- 115 microm preoperatively to 261 +/- 123 microm 2 months after surgery (P = 0.0041). However, 59% of eyes showed recurrence of macular edema during the follow-up period. Twelve eyes with residual or recurrent macular edema received sub-Tenon capsule injections of TA; of these eyes, 9 showed substantial reduction of macular edema. Foveal thickness decreased from 381 +/- 102 microm to 256 +/- 56 microm (P = 0.0076) 2 weeks after postoperative injections of TA. At the final visit, visual acuity (logMAR) improved from 0.74 +/- 0.40 preoperatively to 0.40 +/- 0.34 (P = 0.010). CONCLUSION: An intraoperative injection of TA in combination with PPV has the potential to facilitate the absorption of macular edema associated with BRVO. In addition, residual or recurrent macular edema can be treated with additional sub-Tenon capsule injections of TA.

Aged↗